Regional metabolic status of the E–18 rat fetal brain following transient hypoxia/ischemia
Increasing evidence indicates that fetal metabolic stress may result in a variety of post–natal perturbations during brain development. The goal of the study was to determine the duration of hypoxia/ischemia that would elicit a demonstrable regional depression of metabolism in the fetal brain and further to examine several end–points to determine if the metabolic stress affects the developing brain. The uterine artery and uterine branch of the ovarian artery were occluded with aneurysm clamps for a period of 45 min, the clips removed and the metabolites in five regions of the perinatal brain were measured at 0, 2 and 6 h of reflow. Regional P–creatine, ATP and glucose levels were significantly depleted at the end of the 45 min occlusion. The levels of glycogen and glutamate at the end of the occlusion indicated a decreasing trend which was not significant. The concentration of citrate remained essentially unchanged at the end of the occlusion. To ensure that the insult was not lethal to the tissue, the recovery of the metabolites was examined at 2 and 6 h of reflow and generally the concentrations of the high–energy phosphates and glucose were normal or near–normal by 6 h of reperfusion in the five regions of the brain examined. The changes in the metabolites indicate that 45 min of hypoxia/ischemia is an appropriate model for studying neonatal development after fetal metabolic stress.
KeywordsFetal metabolic Stress Neonatal brain development
Study supported in part by R01 NS 32683 and Philip Morris External Research Program.
- Altman J, Bayer S (1995) Atlas of prenatal rat brain development. CRC Press, Ann Arbor: pp. 389–387Google Scholar
- Anderson ML, Wolpert SM, Kaye EM (1992) Vascular disease and trauma. In: Wolpert SM, Barnes PD (eds) MRI in pediatric neuroradiology, pp. 177–173Google Scholar
- Bulterys M, Greenland S, Krau J (1990) Chronic fetal hypoxia and sudden infant death syndrome: Interaction between maternal smoking and low hematocrit during pregnancy. PedB 86:535–540Google Scholar
- Lowry O, Passonneau J (1972). A flexible system of enzymatic ananlysis. Academic Press Inc., New YorkGoogle Scholar
- Papile LA (1992) Central nervous disturbances, part 4. In: Fanaroff AA, Martin MJ (eds) Neonatal-perinatal medicine-diseases of the fetus and infant. Mosby-Year Book, Inc, pp. 719–728Google Scholar
- Squire M., Keeling J (1991) The incidence of prenatal brain injury. Neuropathol Appl Neurobiol 17:29–38Google Scholar
- Uvebran P, Hagberg G (1992) Intrauterine growth in children with cerebral palsy. Acta Paediatric 81:407–412Google Scholar